Fenofibrate Canon pills 145mg, 30pcs

Composition

of 1 tab. :

– fenofibrate 145 mg

Auxiliary substances:

corn starch-137 mg,

colloidal silicon dioxide-10 mg,

croscarmellose sodium-33 mg,

mannitol-170 mg,

magnesium stearate-6 mg,

povidone K-30-44 mg,

microcrystalline cellulose-105 mg.

Composition of the film shell:

Opadray II white – 20 mg, including polyvinyl alcohol-9.38 mg,

macrogol-4.72 mg,

talc-3.48 mg,

titanium dioxide-2.42 mg

Pharmacological action

Pharmaceutical group:

Hypolipidemic drug.

Pharmaceutical action:

By activating RAPP-alpha (alpha receptors activated by the peroxisome proliferator), fenofibrate enhances lipolysis and elimination of high-triglyceride atherogenic lipoproteins from blood plasma by activating lipoprotein lipase and reducing the synthesis of apoproteins CII. Activation of RAPP-alpha also leads to increased synthesis of apoproteins AI and AII.

Fenofibrate is a derivative of fibroic acid, whose ability to change the lipid content in the human body is mediated by activation of RAPP-alpha. The above-described effects of fenofibrate on lipoproteins lead to a decrease in the content of the low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) fractions, which include apoprotein B, and an increase in the content of the high-density lipoprotein (HDL) fractions, which include apoproteins AI and AII.

In addition, by correcting violations of VLDL synthesis and catabolism, fenofibrate increases LDL clearance and reduces the content of dense and small LDL particles, an increase in which is observed in patients with an atherogenic lipid phenotype, a frequent violation in patients at risk of coronary heart disease. In clinical studies, it was noted that the use of fenofibrate reduces the concentration of total cholesterol by 20-25% and triglycerides by 40-55%, while increasing the concentration of HDL cholesterol by 10-30%. In patients with hypercholesterolemia, in whom the concentration of LDL cholesterol decreases by 20-35%, the use of fenofibrate led to a decrease in the ratios: “total cholesterol/HDL-cholesterol”, “LDL-cholesterol/HDL-cholesterol” and “A by B/A by AI”, which are markers of atherogenic risk.

Given the significant effect on LDL cholesterol and triglyceride concentrations, the use of fenofibrate is effective in patients with hypercholesterolemia, both accompanied and not accompanied by hypertriglyceridemia, including secondary hyperlipoproteinemia, for example, in type 2 diabetes mellitus. During treatment with fenofibrate, extravascular cholesterol deposits (tendon and tuberous xanthomas) can significantly decrease and even completely disappear. Patients with elevated fibrinogen levels treated with fenofibrate showed a significant decrease in this indicator, as well as in patients with elevated lipoprotein levels. Other markers of inflammation, such as C-reactive protein, are also reduced by treatment with fenofibrate.

For patients with dyslipidemia and hyperuricemia, an additional benefit is the uricosuric effect of fenofibrate, which leads to a decrease in uric acid concentration by approximately 25%.

In clinical studies and animal experiments, fenofibrate has been shown to reduce platelet aggregation caused by adenosine diphosphate, arachidonic acid, and epinephrine.

Pharmacokinetics:  

The drug Fenofibrate Canon in the form of micronized fenofibrate has a higher bioavailability. The initial fenofibrate is not detected in the blood plasma. The main plasma metabolite is fenofibroic acid.

Suction:  Cmax is reached 4-5 hours after ingestion. With prolonged use, the concentration of the drug in the blood plasma remains stable. The absorption of fenofibrate increases when taken simultaneously with food.

Distribution:  fenofibroic acid binds strongly to plasma albumin (more than 99%). Half-life: T1 / 2 of fenofibroic acid is about 20 hours.

Metabolism and elimination:  only the main metabolite of fenofibrate, fenofibroic acid, is detected in the blood plasma. Fenofibrate is not a substrate for the CYP3A4 isoenzyme. It does not participate in microsomal metabolism.

It is mainly excreted by the kidneys in the form of fenofibroic acid and glucuronide conyogate. Within 6 days, fenofibrate is almost completely eliminated. The total clearance of fenofibroic acid determined in elderly patients does not change. The drug does not accumulate after a single dose and with prolonged use. It is not excreted during hemodialysis.

Indications

– combined therapy with HMG-COA reductase inhibitors (statins) mixed dyslipidemia (type lla, llb according to Fredrickson), with the aim of lowering triglycerides (TG) and increase the concentration of HDL in patients with CHD or at high risk of coronary heart disease (and other clinical forms of atherosclerotic disease: atherosclerosis of peripheral arteries, abdominal aortic aneurysm, and symptomatic carotid atherosclerosis; diabetes mellitus; multiple risk factors, which correspond to the 10-year risk of coronary events > 20%);

– with the aim of reducing the concentration of TG in patients with severe hyperglyceridemia (dyslipidemia IV, V type according to Fredrickson);

– to reduce high concentration of LDL, total cholesterol, triglycerides, and Apob (apolipoprotein b) and increase the concentration of HDL in patients with primary hyperlipidemia or mixed dyslipidemia (type lla, llb, III, IV according to Fredrickson).

Contraindications

-hypersensitivity to fenofibrate or other components of the drug; – liver failure (including biliary cirrhosis and persistent liver dysfunction of unknown etiology);- severe renal insufficiency (creatinine clearance;- age up to 18 years (efficacy and safety have not been established);- a history of photosensitivity or phototoxicity during treatment with fibrates or ketoprofen;- a history of gallbladder disease;- breast-feeding period;- chronic or acute pancreatitis, except in cases of acute pancreatitis caused by severe hypertriglyceridemia.

With caution: in hypothyroidism; in patients who abuse alcohol; in patients with impaired renal function (creatinine clearance more than 20 ml / min); in the elderly, with a history of hereditary muscle diseases; while taking oral anticoagulants, HMG-CoA reductase inhibitors (see the section “Interaction with other drugs”).

Side effects

Side effects for therapeutic doses are given by frequency and organ-system classes according to the WHO classification: very common – ≥1/10 prescriptions (>10%) often – ≥1/100 to >< 1/10 prescriptions (>1% and 0.1% and < 1/10 prescriptions (>< 1%) rarely – ≥1/10000 to < 1/1000 prescriptions (>0.01% and from the digestive system: often-abdominal pain, nausea, vomiting, diarrhea and flatulence of moderate severity;infrequently-cases of pancreatitis. often-a moderate increase in the concentration of serum transaminases; infrequently-the formation of gallstones;very rarely-hepatitis.

If symptoms of hepatitis (jaundice, pruritus) appear, laboratory tests should be performed and, if hepatitis is confirmed, fenofibrate should be discontinued. (see the section “Special instructions”).

Musculoskeletal and connective tissue disorders: rarely-diffuse myalgia, myositis, muscle spasm and weakness; very rarely-rhabdomyolysis, increased creatine phosphokinase (CPK) activity.

Vascular disorders: infrequently-venous thromboembolism (pulmonary embolism, deep vein thrombosis).

From the circulatory and lymphatic system: rarely-increased hemoglobin and white blood cells.

Nervous system disorders: rarely-sexual dysfunction, headache.

Respiratory system disorders: very rarely – interstitial pneumopathies.

Skin and subcutaneous fat disorders: rarely rash, pruritus, urticaria or reaction photosensitivity;rarely – alopecia;

rarely – photosensitivity, accompanied by erythema, blistering or nodules on the skin areas exposed to sunlight or artificial UV light (e. g., quartz lamps) in some cases (even after months of use without any complications).

Laboratory tests: infrequently-increased serum creatinine and urea concentrations.

Interaction

Oral anticoagulants:

Fenofibrate enhances the effect of oral anticoagulants and may increase the risk of bleeding, which is associated with the displacement of the anticoagulant from the sites of binding to plasma proteins.

At the beginning of treatment with fenofibrate, it is recommended to reduce the dose of anticoagulants by approximately one third, followed by a gradual dose adjustment. Dose selection is recommended to be carried out under the control of the INR level (international normalized ratio).

Cyclosporine: Several severe cases of reversible renal impairment have been reported during concomitant treatment with fenofibrate and cyclosporine. Therefore, it is necessary to monitor the state of renal function in such patients and discontinue fenofibrate in case of serious changes in laboratory parameters.

HMG-CoA reductase inhibitors (statins) and other fibrates:

Taking fenofibrate concomitantly with HMG-CoA reductase inhibitors or other fibrates increases the risk of serious toxic effects on muscle fibers (see section “Special instructions”).

Cytochrome P isoenzymes%^%450:

In vitro studies of human liver microsomes have shown that fenofibrate and fenofibroic acid are not inhibitors of the following cytochrome P 450 isoenzymes (CYP3A4, CYP2D6, CYP2E1, or CYP1A2). At therapeutic concentrations, these compounds are weak inhibitors of the CYP2C19 and CYP2A6 isoenzymes and weak or moderate inhibitors of CYP2C9.

How to take, course of use and dosage

Tablets should be swallowed whole, without chewing, at the same time as a meal.

Adults:Take one tablet once a day. Patients taking one capsule of fenofibrate 200 mg can switch to one tablet of Fenofibrate Canon 145 mg without additional dose adjustment. The maximum daily dose is 145 mg.

Elderly patients:It is recommended to take 1 tablet of 145 mg for adults (one tablet once a day).

Patients with liver diseases:The use of the drug in patients with liver diseases has not been studied.

The drug should be taken for a long time, while continuing to follow the diet that the patient followed before starting treatment with Fenofibrate Canon.

Overdose

Cases of overdose are not described.

The specific antidote is unknown.

If an overdose is suspected, symptomatic and, if necessary, supportive treatment should be prescribed.

Hemodialysis is ineffective.

Special instructions

Before starting treatment with Fenofibrate Canon, appropriate treatment should be performed to eliminate the cause of secondary hypercholesterolemia, for example, in diseases such as uncontrolled type 2 diabetes, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver diseases, consequences of drug therapy, alcoholism.

The effectiveness of therapy should be evaluated by the content of lipids (total cholesterol, LDL, triglycerides) in the blood serum. If there is no therapeutic effect after several months of therapy (usually after 3 months), the expediency of prescribing concomitant or alternative therapy should be considered.

In patients with hyperlipidemia who are taking estrogens or hormonal contraceptives containing estrogens, it is necessary to determine whether the hyperlipidemia is of a primary or secondary nature. In such cases, an increase in the level of lipids can be caused by taking estrogens.

Liver function: when taking fenofibrate and other drugs that reduce lipid concentrations, in some patients, an increase in the activity of “hepatic” transaminases has been described. In most cases, this increase was temporary, insignificant, and asymptomatic. During the first 12 months of treatment, it is recommended to monitor the activity of transaminases (alanine aminotransferase (ALT), aspartate aminotransferase (ACT)) every 3 months. Patients who have increased transaminase concentrations during treatment require attention, and in case of an increase in ALT and ACT concentrations by more than 3 times compared to the upper limit of normal, the drug is discontinued.

Pancreatitis: Cases of pancreatitis have been reported during treatment with fenofibrate. Possible causes of pancreatitis in these cases were: insufficient efficacy of the drug in patients with severe hypertriglyceridemia, direct exposure to the drug, as well as secondary phenomena associated with the presence of stones or sediment formation in the gallbladder, accompanied by obstruction of the common bile duct.

Muscle: when taking fenofibrate and other medications that reduce lipid concentrations, cases of toxic effects on muscle tissue have been described, including very rare cases of rhabdomyolysis. The frequency of this disorder increases in the case of hypoalbuminemia and a history of renal failure. The possibility of this complication increases in cases of hypoalbuminemia and renal failure.

Toxic effects on muscle tissue may be suspected based on patient complaints of weakness, diffuse myalgia, myositis, muscle spasms and convulsions, and / or a marked increase in creatinine phosphokinase (CPK) activity (more than 5 times higher than the upper limit of normal). In these cases, treatment with fenofibrate should be discontinued.

The risk of developing rhabdomyolysis may be increased in patients with a predisposition to myopathy and/or rhabdomyolysis, including those over 70 years of age, a history of hereditary muscle diseases, impaired renal function, hypothyroidism, and alcohol abuse. Such patients should be prescribed the drug only if the expected benefit exceeds the possible risk of developing rhabdomyolysis. When taking Fenofibrate Canon concomitantly with HMG-CoA reductase inhibitors or other fibrates, the risk of serious toxic effects on muscle fibers increases, especially if the patient suffered from muscle disease before starting treatment. In this regard, the combined use of Fenofibrate Canon and statiya is permissible only if the patient has severe mixed dyslipidemia and a high cardiovascular risk, in the absence of a history of muscle disease and in conditions of close monitoring aimed at detecting signs of toxic effects on muscle tissue.

Renal function: When using Fenofibrate Canon as monotherapy or in combination with statins, a reversible increase in serum creatinine concentrations was observed in patients. The increase in creatinine concentration was generally stable over time with no signs of further increase in serum creatinine concentrations during long-term therapy, with a tendency to return to initial values after discontinuation of treatment. The clinical significance of these observations has not been established. In patients with renal insufficiency, monitoring of renal function is recommended when taking Fenofibrate Canon. Monitoring of renal function should be performed in patients at risk of developing renal failure, namely elderly patients and patients with diabetes mellitus. Treatment should be discontinued if the creatinine concentration increases > 50% of the upper limit of normal. It is recommended to determine the creatinine concentration during the first 3 months after the start of treatment, as well as periodically after its end.

Influence on the ability to drive a car and other mechanisms:

When using the drug, there was no effect on the ability to drive a car and other mechanisms.

Active ingredient

Fenofibrate

Conditions of release from pharmacies

By prescription

Dosage form

Tablets

Purpose

For adults as directed by your doctor

Indications

Atherosclerosis